U.S. patent application number 11/097706 was filed with the patent office on 2006-10-05 for method and apparatus for evaluating ventricular performance during isovolumic contraction.
Invention is credited to David E. Euler, Douglas A. Hettrick.
Application Number | 20060224203 11/097706 |
Document ID | / |
Family ID | 36950445 |
Filed Date | 2006-10-05 |
United States Patent
Application |
20060224203 |
Kind Code |
A1 |
Hettrick; Douglas A. ; et
al. |
October 5, 2006 |
Method and apparatus for evaluating ventricular performance during
isovolumic contraction
Abstract
A method of evaluating ventricular performance of a heart
employing sensors to measure a ventricular dimension signal and
deriving indices of ventricular performance therefrom. Premature
Shortening (PS) and Isovolumic Lengthening (IL) comprise two
indices of ventricular performance determined from analysis of the
left ventricular dimension signal during the transition from
ventricular filling to ventricular ejection. Measured values of PS
and IL are compared to other measured values or reference values to
determine if ventricular performance has improved (or worsened). In
some embodiments, the dimension sensors may comprise piezoelectric
sonomicrometer crystals that operate as ultrasound transmitters and
receivers. The sensors may be mounted in relation to a ventricle of
the heart either temporarily or permanently, and may be configured
either separately from or integrally with cardiac pacing leads.
Inventors: |
Hettrick; Douglas A.;
(Blaine, MN) ; Euler; David E.; (Maple Grove,
MN) |
Correspondence
Address: |
MEDTRONIC, INC.
710 MEDTRONIC PARK
MINNEAPOLIS
MN
55432-9924
US
|
Family ID: |
36950445 |
Appl. No.: |
11/097706 |
Filed: |
March 31, 2005 |
Current U.S.
Class: |
607/19 |
Current CPC
Class: |
A61N 1/3627 20130101;
A61N 1/36843 20170801; A61N 1/36842 20170801; A61N 1/3684 20130101;
A61B 8/0858 20130101; A61N 1/36528 20130101 |
Class at
Publication: |
607/019 |
International
Class: |
A61N 1/365 20060101
A61N001/365 |
Claims
1. A method of evaluating the ventricular performance of a heart
comprising: positioning a first sensor at a first location of the
heart, and a second sensor at a second location of the heart, the
first and second locations spanning a portion of a ventricle;
measuring a distance between the first and second sensors over a
cardiac cycle of the heart to produce a ventricular dimension
signal as a function of time, the cardiac cycle comprising a
ventricular filling phase and a ventricular ejection phase;
measuring at least one of the following values: a) premature
shortening (PS) of the ventricular dimension signal, the value of
PS being equal to the decrease in the ventricular dimension signal
from a first local maximum value that occurs at or near an end of
the ventricular filling phase of the cardiac cycle, to a relative
minimum value or inflection point that occurs during a transition
from the ventricular filling phase to the ventricular ejection
phase of the cardiac cycle; and b) isovolumic lengthening (IL) of
the ventricular dimension signal, the value of IL being equal to
the increase in the ventricular dimension signal from the relative
minimum value or inflection point that occurs during the transition
from the ventricular filling phase to the ventricular ejection
phase of the cardiac cycle, to a second local maximum value that
occurs at or near a beginning of the ventricular ejection phase of
the cardiac cycle; and comparing the at least one measured value of
PS or IL with at least one reference value or at least one
previously measured value of PS or IL.
2. The method of claim 1 wherein a decrease in the at least one
measured value of PS or IL with respect to the at least one
reference value or the at least one previously measured value of PS
or IL generally indicates an improvement in the ventricular
performance of the heart.
3. The method of claim 2 wherein a value of approximately zero for
PS and IL indicates an optimum level of ventricular performance of
the heart.
4. The method of claim 2 wherein a decrease in a sum of the
measured values of PS and IL indicates an improvement in the
ventricular performance of the heart.
5. The method of claim 1 wherein the first and second sensors are
sonomicrometry crystals.
6. The method of claim 5 wherein the sonomicrometry crystals use
the piezoelectric effect to transmit and receive sound energy.
7. The method of claim 1 wherein an electromagnetic energy signal
is emitted from one of the first and second sensors that causes the
other of the first and second sensors to sense the electromagnetic
energy signal a time delay later, and wherein the distance between
the first and second sensors is a function of the time delay
between the emitted and sensed electromagnetic energy signal.
8. The method of claim 1 wherein one of the first and second
sensors is positioned generally near a right ventricular apex of
the heart, and wherein the other of the first and second sensors is
positioned in or near the coronary sinus of the heart.
9. The method of claim 1 further comprising measuring the value of
at least one of PS and IL over a plurality of cardiac cycles and
determining a weighted average value of at least one of PS and IL
for comparison to at least one reference value or at least one
previously measured value of PS or IL.
10. The method of claim 1 further comprising: determining the value
of the first local maximum, the relative minimum, and the second
local maximum of the ventricular dimension signal by a method that
includes identifying when a first derivative of the ventricular
dimension signal changes polarity.
11. The method of claim 1 further comprising: determining the value
of the first local maximum, the relative minimum, and the second
local maximum of the ventricular dimension signal by a method that
includes correlation of the ventricular dimension signal with zero
crossings of a first derivative of the ventricular dimension
signal.
12. The method of claim 1 wherein the heart is operatively coupled
to an Implantable Medical Device (IMD) comprising a plurality of
leads and device circuitry, the method further comprising: storing
measured values of at least one of PS and IL in the IMD for
comparison to at least one reference value or at least one other
measured value of PS or IL to monitor and evaluate changes in the
ventricular performance of a heart.
13. The method of claim 12 further comprising: adjusting the
operation of the IMD in response to the measured values of at least
one of PS and IL to attempt to reduce subsequent measured values
and thereby improve the ventricular performance of a heart.
14. The method of claim 13 wherein the IMD stimulates one or a
combination of the right atrium, right ventricle, and left
ventricle, the method further comprising adjusting a pacing
parameter to attempt to reduce at least one of PS and IL and
thereby improve the ventricular performance of a heart.
15. The method of claim 14 wherein the pacing parameter adjusted is
the atrio-ventricular (AV) delay.
16. The method of claim 14 wherein the pacing parameter adjusted is
the inter-ventricular (VV) delay.
17. The method of claim 13 wherein the IMD includes the ability to
pace from multiple pacing site locations on at least one pacing
lead, the method further comprising: adjusting the pacing site
location to attempt to reduce at least one of PS and IL and thereby
improve the ventricular performance of a heart.
18. The method of claim 1 wherein the heart is operatively coupled
to at least one pacing lead, the method further comprising: storing
measured values of at least one of PS and IL at a given
configuration of lead locations; repositioning the at least one
pacing lead; storing measured values of at least one of PS and IL
at a second and subsequent configurations of lead locations; and
adjusting the placement of pacing leads to minimize the measured
values and thereby optimize the ventricular performance of a
heart.
19. A method of operating an implantable medical device having a
plurality of leads and having an implantable medical device circuit
enclosed within a hermetically sealed housing, the method
comprising: implanting a first lead bearing a first sonomicrometer
crystal at a first location of the heart; implanting a second lead
bearing a second sonomicrometer crystal at a second location of the
heart, the first and second locations spanning a portion of the
left ventricle; coupling the first and second leads to the
implantable medical device circuit and implanting the housing in a
patient; and operating the implantable medical device by: during
one or more heart cycles, periodically energizing one of the first
and second sonomicrometer crystals to emit an ultrasonic frequency
emitted signal that causes the other of the first and second
sonomicrometer crystals to develop an ultrasonic frequency sense
signal; determining the distance between the first and second
sonomicrometer crystals as a function of the time delay between
emission of the emitted signal and sensing of the respective sense
signal; measuring at least one of the following values: a)
premature shortening (PS) of the ventricular dimension signal, the
value of PS being equal to the decrease in the ventricular
dimension signal from a first local maximum value that occurs at or
near an end of the ventricular filling phase of the cardiac cycle,
to a relative minimum value or inflection point that occurs during
a transition from the ventricular filling phase to the ventricular
ejection phase of the cardiac cycle; and b) isovolumic lengthening
(IL) of the ventricular dimension signal, the value of IL being
equal to the increase in the ventricular dimension signal from the
relative minimum value or inflection point that occurs during the
transition from the ventricular filling phase to the ventricular
ejection phase of the cardiac cycle, to a second local maximum
value that occurs at or near a beginning of the ventricular
ejection phase of the cardiac cycle; comparing the at least one
measured value of PS or IL with at least one reference value or at
least one other measured value of PS or IL; and adjusting the
operation of the implantable medical device.
20. An implantable medical device (IMD) for evaluating ventricular
performance of a heart comprising: a plurality of leads and an
implantable medical device circuit enclosed within a hermetically
sealed housing; a first lead bearing a first sonomicrometer crystal
adapted to be positioned at a first location of the heart; a second
lead bearing a second sonomicrometer crystal adapted to be
positioned at a second location of the heart, the first and second
locations spanning a portion of the left ventricle, the first and
second leads adapted to be coupled to the IMD circuit, the housing
of the IMD adapted to be implanted in a patient, and the IMD
capable of: periodically energizing one of the first and second
sonomicrometer crystals during one or more heart cycles to emit an
ultrasonic frequency emitted signal that causes the other of the
first and second sonomicrometer crystals to develop an ultrasonic
frequency sense signal; determining the distance between the first
and second sonomicrometer crystals as a function of the time delay
between emission of the emitted signal and sensing of the
respective sense signal; measuring at least one of the following
values: a) premature shortening (PS) of the ventricular dimension
signal, the value of PS being equal to the decrease in the
ventricular dimension signal from a first local maximum value that
occurs at or near an end of the ventricular filling phase of the
cardiac cycle, to a relative minimum value or inflection point that
occurs during a transition from the ventricular filling phase to
the ventricular ejection phase of the cardiac cycle; and b)
isovolumic lengthening (IL) of the ventricular dimension signal,
the value of IL being equal to the increase in the ventricular
dimension signal from the relative minimum value or inflection
point that occurs during the transition from the ventricular
filling phase to the ventricular ejection phase of the cardiac
cycle, to a second local maximum value that occurs at or near a
beginning of the ventricular ejection phase of the cardiac cycle;
comparing the at least one measured value of PS or IL with at least
one reference value or at least one other measured value of PS or
IL; and adjusting the operation of the implantable medical device.
Description
FIELD OF THE INVENTION
[0001] Embodiments of the invention relate generally to implantable
medical devices (IMDS) that deliver therapies to the heart and/or
monitor cardiac physiologic parameters. More particularly,
embodiments of the invention relate to the use of sensors
positioned in relation to the heart to monitor physical dimensions
of the heart and to collect, derive and utilize information
regarding cardiac performance for therapeutic and diagnostic
purposes.
BACKGROUND OF THE INVENTION
[0002] A wide variety of IMDs have been developed over the years or
are proposed that provide cardiac rhythm management of disease
states manifested by cardiac rhythm disorders and heart failure.
Implantable pacemakers have been developed that monitor and restore
heart rate and rhythm of patients that suffer bradycardia (too-slow
or irregular heart rate), tachycardia (regular but excessive heart
rate), and heart failure (the inability of the heart to maintain
its workload of pumping blood to the body). Implantable
cardioverter-defibrillators (ICDs) have been developed that deliver
programmed cardioversion/defibrillation shocks to the atria, in
response to detection of atrial fibrillation (rapid, uncontrolled
heartbeats in the atria), or to the ventricles, in response to
life-threatening, ventricular tachyarrhythmias. Typically, single
and dual chamber bradycardia pacing systems are also incorporated
into ICDs.
[0003] Cardiac IMDs have traditionally employed the ability to
detect or sense electrical activity in the heart as the basis for
determining and delivering appropriate therapy. For example,
appropriately placed electrical sensors may sense the contractions
of the atria and/or the ventricles as evidenced by P-waves and
R-waves detected in atrial and ventricular electrogram (EGM)
signals, respectively. The timing of detected atrial and
ventricular contractions (sensed events) may be used by the IMD to
monitor for and treat cardiac arrhythmias such as bradycardia,
tachycardia, and fibrillation.
[0004] Among the earliest cardiac rhythm management IMDs were
single-chamber, fixed-rate pacing systems comprising an implantable
pulse generator (IPG) and a lead bearing one or more pace/sense
electrodes adapted to be placed in contact with the heart chamber
to be paced. These IMDs, commonly referred to as pacemakers,
provided fixed-rate pacing to a single heart chamber when the heart
rate fell below a programmable lower rate limit.
[0005] Another cardiac rhythm management IMD, the implantable
cardioverter defibrillator ("ICD"), was developed for treating
abnormally fast heart rhythms. The earliest ICDs delivered a
defibrillation shock to the ventricles when heart rate, as
determined by sensed ventricular contractions, and certain other
criteria were met. It was proposed that blood pressure sensors or
accelerometers be incorporated in ICDs so that the absence of
mechanical heart function during fibrillation could also be
detected to confirm the presence of fibrillation before a shock
therapy was delivered.
[0006] Over the years, pacemakers and ICDs have evolved in
complexity and capabilities. Increasingly complex signal processing
algorithms have been developed to evaluate electrogram (EGM)
signals and to thereby attempt to provide the most appropriate
therapy to restore a normal heart rhythm and to avoid delivery of
inappropriate therapy that may be painful and potentially harmful
to the patient.
[0007] It has been recognized that other indicators of heart
function, particularly indicators related to mechanical heart
function, would be of great value in augmenting the algorithms that
process atrial and ventricular EGM signals in order to resolve
ambiguities that may arise. It is desirable, for example, to know
whether a delivered pacing pulse has "captured" the heart, i.e.,
caused the heart chamber to contract. Similarly, it is desirable to
rapidly determine whether a delivered cardioversion/defibrillation
shock has effectively terminated a tachyarrhythmia and whether the
heart has returned to a normal rhythm.
[0008] There are other situations where it would be useful to
incorporate measurements or indications of mechanical heart
function in pacing systems. For example, patients suffering from
chronic heart failure or congestive heart failure (CHF) often
manifest an elevation of left ventricular end-diastolic pressure.
This may occur while left ventricular end-diastolic volume remains
normal due to a decrease in left ventricular compliance. CHF due to
chronic hypertension, ischemia, infarct or idiopathic
cardiomyopathy may be associated with compromised systolic and
diastolic function involving decreased atrial and ventricular
muscle compliance. These conditions may be associated with chronic
disease processes, or complications from cardiac surgery with or
without specific disease processes. Most heart failure patients
suffer from conditions which may include a general weakening of the
contractile function of the cardiac muscle, attendant enlargement
thereof, impaired myocardial relaxation, and depressed ventricular
filling characteristics in the diastolic phase following
contraction. Pulmonary edema, shortness of breath, and disruption
in systemic blood pressure are symptoms associated with acute
exacerbations of heart failure.
[0009] These disease processes often lead to insufficient cardiac
output to sustain mild or moderate levels of exercise and proper
function of other body organs; progressive worsening eventually
results in cardiogenic shock, arrhythmias, electromechanical
dissociation, and death. In order to monitor the progression of the
disease and to assess efficacy of prescribed treatment, it is
desirable to obtain accurate measures of the heart geometry, and
the mechanical pumping capability of the heart, under a variety of
metabolic conditions. These parameters have typically been measured
through the use of external echocardiogram equipment in a clinical
setting. However, the measurement procedure is time consuming and
expensive to perform for even a resting patient, and cannot be
practically performed while replicating a range of metabolic
conditions. Typically, the echocardiography procedure is performed
infrequently, and months or years may lapse between successive
tests, resulting in a poor understanding of the progress of the
disease or whether or not intervening therapies have been
efficacious. Quite often, only anecdotal evidence from the patient
is available to gauge the efficacy of the prescribed treatment.
[0010] It has been proposed to employ sensors that respond to
mechanical activity of the heart to provide an indication of the
strength, velocity or range of motion of one or more of the heart
chambers or valves. It is desirable that such information
complement information obtained from EGM signals to more
confidently detect arrhythmias or trigger delivery of appropriate
therapies. It is also desirable to derive indicators of intrinsic
cardiac performance and response to delivered therapies that can be
employed to confirm or adjust therapy delivery, or to indicate the
state and progress of the underlying cardiac disease.
[0011] It has been proposed to employ permanently implantable
sensors that provide a more direct measure of mechanical motion of
muscle mass or particular structures of the heart, including the
opening and closing of heart valves and the motion or deformation
of the septal wall and the ventricular and atrial walls. Such
sensors include intracardiac pressure sensors, accelerometers,
impedance measurement electrode systems, and Doppler motion
sensors.
[0012] As noted in U.S. Pat. No. 5,544,656, measurement of
myocardial wall thickness, as well as end-systolic and
end-diastolic dimensions, may be useful in evaluating the effects
of changes in regional myocardial function and contractility,
including evaluating myocardial oxygen supply and demand, in acute
and chronic animal studies. A transit-time sonomicrometry system is
disclosed in the background of the '656 patent that uses two
piezoelectric crystals, one as a transmitter and the other as a
receiver, and operates by measuring the time required for
ultrasound to travel between the transmitting and receiving
transducers. An advantage of this system is its ability to provide
an absolute dimension signal output calibrated in units of
distance.
[0013] The '656 patent also discloses a closed-loop,
single-crystal, ultrasonic sonomicrometer capable of identifying
the myocardial muscle/blood interface and continuously tracking
this interface throughout the cardiac cycle using a piezoelectric
transducer that operates in the manner of a Doppler echo sensor
implanted at least partly in the myocardium and partly in the blood
within a heart chamber.
[0014] Sonomicrometer systems that are installed epicardially about
the heart to measure heart movement across a number of vectors are
also disclosed in the article "Miniature Implantable Sonomicrometer
System," by Robert D. Lee et al., (Journal of Applied Physiology,
Vol. 28, No. 1, January 1970, pp. 110-112), in EP0 467 695 A2, and
in PCT publication WO 00/69490. The Lee article describes an
implantable monitoring system attached to the epicardial
electrodes. Invasive surgery is necessary to expose locations where
sonomicrometer crystals may be surgically attached to the
epicardium.
[0015] Some of the various chronically implanted sensors described
above are intended to be incorporated into lead bodies that are
typically introduced transvenously into the relatively low pressure
right heart chamber or blood vessels accessible from the right
atrium through the patient's venous system. The introduction of
such sensors into left heart chambers through the arterial system
introduces complications that may be difficult to manage both
acutely and chronically. The surgical approach to the exterior of
the heart is also not favored as it may complicate the surgery and
recovery of the patient. However, measurement of left heart
function remains desirable in a number of clinical cases including
chronic heart failure.
[0016] Stadler et al. (U.S. Pat. No. 6,795,732) discloses a system
and method for determining mechanical heart function and measuring
mechanical heart performance of both left and right heart chambers
without intruding into a left heart chamber or requiring invasive
surgery to access the epicardium of the left heart chamber. The
system disclosed by Stadler et al. may be incorporated in IMDs (for
therapy delivery) and/or implantable monitoring devices employing
dimension sensors, such as piezoelectric sonomicrometry crystals.
U.S. Pat. No. 6,795,732 to Stadler et al. is assigned to the
present assignee and is hereby incorporated by reference in its
entirety.
[0017] The dimension sensors of Stadler et al. comprise at least a
first sonomicrometer piezoelectric crystal mounted to a first lead
body implanted into or in relation to one heart chamber, e.g., the
right ventricle (RV), that operates as an ultrasound transmitter
when a drive signal is applied to it or as an ultrasound receiver,
and at least one second sonomicrometer crystal mounted to a second
lead body implanted into or in relation to a second heart chamber,
e.g., the left ventricle (LV), the left atrium (LA), or the right
atrium (RA), that operates as an ultrasound receiver or as an
ultrasound transmitter when a drive signal is applied to it,
respectively. The ultrasound receiver converts impinging ultrasound
energy transmitted from the ultrasound transmitter through blood
and heart tissue into an electrical signal. The time delay between
the generation of the transmitted ultrasound signal and the
reception of the ultrasound wave varies as a function of distance
between the ultrasound transmitter and receiver, which in turn
varies with contraction and expansion of a heart chamber between
the first and second sonomicrometer crystals. One or more
additional sonomicrometer piezoelectric crystals can be mounted to
additional lead bodies, such that the distances between the three
or more sonomicrometer crystals can be determined. In each case,
the sonomicrometer crystals are distributed about a heart chamber
of interest such that the distance between the separated ultrasound
transmitter and receiver crystal pairs changes with contraction and
relaxation of the heart chamber.
[0018] The RV-LV distance between the RV and LV crystals of Stadler
et al. is a measure of LV dimension. Changes in the LV dimension
over the cardiac cycle are correlated with changes in LV volume as
the LV fills during diastole and empties during systole. The LV-RA
distance between the LV and RA crystals varies as a function of RA
mechanical activity as the RA fills and empties in a pattern during
normal sinus rhythm that markedly differs from the pattern
exhibited during atrial fibrillation and other forms of ineffective
atrial contraction. The RV-RA distance and RV-LA distance between
the RV sonomicrometer crystal and the respective RA and LA
sonomicrometer crystals varies as a function of a mixture of atrial
and ventricular activity.
[0019] Stadler et al. discloses incorporating sonomicrometer
piezoelectric crystals into cardiac leads, distributing
sonomicrometer piezoelectric crystals about the heart chambers, and
incorporating a control and measurement system in the operating
system of an IMD that measures the distance between the
sonomicrometer crystals as the heart expands and contracts over
each heart cycle. First and second cardiac pacing leads or
cardioversion/defibrillation leads bearing first and second
sonomicrometer crystals, respectively, are implanted through the
coronary sinus (CS) and into the great cardiac vein along the LV
and in the RV apex, respectively. The lead conductors are coupled
to emission, reception, and dimension measurement circuitry within
an IMD IPG or monitor that drives one selected piezoelectric
crystal as an emitter or generator and the other piezoelectric
crystals as receivers, whereby the distances between the crystal
pairs can be measured as a function of the measured transit time
for the transmitted signal to be received by multiplying the time
of travel by the speed of sound in the tissue.
[0020] Stadler et al. also discloses incorporating a sonomicrometer
crystal into a pacing lead with two or more conductors such that
the crystal is wired in parallel with two of the conductors in the
lead. For example, a crystal could be wired in parallel with the
ring and tip pace/sense electrodes of a pacing lead. The ultrasound
crystal has very low impedance to signals near its resonance
frequency (near 1 MHz), and very high impedance to lower frequency
signals. Pacing pulses, which contain lower frequencies, would
preferentially be delivered to the tissue via the tip and ring
electrodes, whereas high frequency pulses to excite the ultrasound
crystal would be preferentially delivered to the crystal.
Additionally, the low pass filter of the pacing sense amplifier
does not pass the very high frequency ultrasound signals emitted by
the crystals. Thus, the sonomicrometer function does not interfere
with normal pacing and sensing functions. As an alternative
implementation, the pacing pulse could be delivered simultaneously
to the tip and ring pace/sense electrodes, with the IPG case or can
as an anode, thereby delivering an effective pacing pulse without
any energy dissipation through the ultrasound crystal. As a second
alternative, filtering circuitry could be incorporated into the
lead to ensure delivery of pacing pulses to the pace/sense
electrodes and ultrasound pulses to the crystals.
[0021] Pacing therapies delivered by implantable devices may, in
some cases, cause asynchronous left ventricular contraction,
particularly when pacing the right ventricular apex. In contrast,
left ventricular, multi-site, or alternative site right ventricular
pacing may lessen the asynchrony of left ventricular contraction
(i.e., improve synchrony of left ventricular contractions). The
ability of these pacing therapies to resynchronize ventricular
contractions may depend on the precise pacing site locations, as
well as on pacing parameters such as the programmed AV delay, VV
delay interval, and possibly other programmable pacing parameters.
However, no clinically accepted method currently exists to reliably
evaluate and optimize cardiac performance using sensors in
conjunction with an implantable device.
BRIEF SUMMARY OF THE INVENTION
[0022] Certain embodiments of the invention provide a method for
evaluating and monitoring ventricular performance using indices of
ventricular performance derived from cardiac dimension signals
obtained from sensors incorporated into permanent pacing leads,
temporary guide wires or catheters, or passive transducers
surgically placed for such purpose without a catheter.
[0023] Certain embodiments of the invention provide a method of
operating an IMD to evaluate and monitor ventricular performance
using indices of ventricular performance derived from LV dimension
measurements, and using the information to optimize ventricular
performance by adjusting the operation of the IMD. IMD adjustments
may include changing programmed pacing parameters, such as AV delay
and V-V delay (in bi-ventricular pacing systems), or by adjusting
pacing site location.
[0024] Certain embodiments of the invention provide an IMD adapted
to evaluate and monitor ventricular performance using indices of
ventricular performance derived from LV dimension measurements. The
IMD may be adjusted manually, for example by an operator via
programmer telemetry commands based on information stored in the
IMD, or the adjustment may be automatic, based on an algorithmic
response to measured indices of ventricular performance.
[0025] This summary of the invention and the objects, advantages
and features thereof have been presented here simply to point out
some of the ways that the invention overcomes difficulties
presented in the prior art and to distinguish the invention from
the prior art and is not intended to operate in any manner as a
limitation on the interpretation of claims that are presented
initially in the patent application and that are ultimately
granted.
BRIEF DESCRIPTION OF THE DRAWINGS
[0026] FIG. 1 is a diagram of a heart with sensors positioned to
measure left ventricular dimension (LV Dim) in accordance with an
embodiment of the invention.
[0027] FIG. 2 is a diagram of a heart and an implantable medical
device (IMD) coupled to pacing leads and sensors located in the
heart according to an embodiment of the invention.
[0028] FIG. 3 is a timing diagram showing the relationship between
the ECG signal during a cardiac cycle and various mechanical
properties associated with heart movement during a cardiac
cycle.
[0029] FIG. 4 is a diagram of LV Dim over time and the first
derivative of LV Dim with respect to time as measured according to
an embodiment of the invention.
[0030] FIG. 5 is a plot of LV Pressure vs. LV Volume for a normal
heart over a cardiac cycle.
[0031] FIG. 6 is a plot of LV Pressure vs. LV Volume over a cardiac
cycle for a number of different pacing site
locations/configurations.
[0032] FIG. 7 is an enlarged view of LV Dim, illustrating the
measurement of two indices of cardiac performance in accordance
with an embodiment of the invention.
[0033] FIG. 8 is an enlarged plot of LV Pressure vs. LV Dim,
showing the corresponding shape change associated with Premature
Shortening (PS) in accordance with an embodiment of the
invention.
[0034] FIG. 8a is an enlarged plot of LV Pressure vs. LV Dim,
showing the corresponding shape change associated with Premature
Shortening (PS) and Isovolumic Lengthening (IL) in accordance with
an embodiment of the invention.
[0035] FIG. 9 is a series of plots of LV Dim showing the effect of
varying the paced AV Delay on the measured value of PS according to
an embodiment of the invention.
[0036] FIG. 10 is a plot of LV Pressure vs. LV Volume over a
cardiac cycle for a number of different pacing site locations and
pacing mode configurations.
[0037] FIG. 11 is a diagram of a heart with multi-site pacing leads
implanted according to an embodiment of the invention.
[0038] FIG. 12 is a diagram of a heart showing a method of
positioning a RV pacing lead using information from temporary
sensors according to an embodiment of the invention.
[0039] FIG. 13 is a diagram of a heart showing a method of
positioning a LV pacing lead using information from temporary
sensors according to an embodiment of the invention.
[0040] FIG. 14 is a block diagram of a method for automatically
adjusting pacing parameters in an IMD according to an embodiment of
the invention.
[0041] FIG. 15 is a diagram of an exemplary programmer screen for
monitoring cardiac performance and manually adjusting pacing
parameters according to an embodiment of the invention.
DETAILED DESCRIPTION OF THE ILLUSTRATED EMBODIMENTS
[0042] The following discussion is presented to enable a person
skilled in the art to make and use the invention. Various
modifications to the illustrated embodiments will be readily
apparent to those skilled in the art, and the generic principles
herein may be applied to other embodiments and applications without
departing from the spirit and scope of the present invention as
defined by the appended claims. Thus, the present invention is not
intended to be limited to the embodiments shown, but is to be
accorded the widest scope consistent with the principles and
features disclosed herein. The following detailed description is to
be read with reference to the figures, in which like elements in
different figures have like reference numerals. The figures, which
are not necessarily to scale, depict selected embodiments and are
not intended to limit the scope of the invention. Skilled artisans
will recognize the examples provided herein have many useful
alternatives which fall within the scope of the invention.
[0043] In the following detailed description, references are made
to illustrative embodiments for carrying out the invention. It is
understood that other embodiments may be utilized without departing
from the scope of the invention. For example, the invention is
disclosed in detail herein in the context of an AV sequential,
three chamber or four chamber, pacing system operating in demand,
atrial tracking, and triggered pacing modes for restoring synchrony
in depolarizations and contraction of left and right ventricles in
sequence with atrial sensed and paced events for treating heart
failure and/or bradycardia in those chambers. This embodiment of
the invention is programmable to operate as a three or four chamber
pacing system having an AV synchronous operating mode for restoring
upper and lower heart chamber synchronization and right and left
atrial and/or ventricular chamber depolarization synchrony.
[0044] It should be appreciated that the present invention may also
be utilized in other embodiments, such as an implantable monitor to
gather data in patients suffering from various forms of heart
failure. The system of the present invention may also be
incorporated into an anti-tachyarrhythmia system including specific
high rate pacing and cardioversion shock therapies associated with
typical implantable cardioverter defibrillators (ICDs) for
providing staged therapies to treat tachyarrhythmias and optionally
including bradycardia pacing systems as are known in the art.
[0045] It will be therefore understood that the various uses of the
dimension signals, and the indices of cardiac performance derived
therefrom, can be employed separately or in various combinations in
multi-site monitoring, pacing and/or ICD systems and can
alternatively be used in simpler dual-chamber and single-chamber
pacemakers, monitors and ICDs which may comprise components of the
embodiment of the invention illustrated herein.
[0046] Embodiments of the invention are therefore not limited to
cardiac resynchronization therapy (CRT) devices, and may be
employed in many various types of implantable cardiac devices.
However, for purposes of illustration only, the invention is
described below in the context of a CRT device having
bi-ventricular pacing capabilities.
[0047] FIG. 1 illustrates the basic sonomicrometry technique
disclosed by Stadler et al. for measuring LV Dim as a function of
time. As shown, sensors such as piezoelectric sonomicrometer
crystals, are placed in two locations that span a portion of the
left ventricle. Other types of sensors having the ability to
transmit and receive energy may also be used. Acoustic,
fibre-optic, infrared, x-ray, RF, and many other forms of
electromagnetic energy may be envisioned as having the ability to
be employed as a sensor for use in measuring LV Dim. The LV Dim
signal is produced by measuring the time delay between sending and
receiving energy, and converting the time delay to distance by
multiplying by the speed of the signal.
[0048] The locations for placement of the sensors may be as shown
in FIG. 1, where sensors are placed in the right ventricular apex
and the distal coronary sinus using a lead or guide wire or guide
catheter. Alternate locations may also be chosen, for example
placing sensors on the outside of the heart using epicardial leads
such that the two sensors span a portion of the left ventricle, or
placing transducers directly on the epicardium or endocardium
without a specific pacing lead. Once positioned, the two sensors
should remain in fixed locations relative to the heart such that
measurements of LV Dim share a common reference and can be
compared. However, it is also envisioned that sensors may become
dislodged or may be intentionally repositioned at a later time, and
that a new reference or baseline LV Dim signal would be
generated.
[0049] FIG. 1 also illustrates the basic theory that may be used to
measure the LV Dim signal using sonomicrometry crystals as the
sensors. An electric potential is applied to one of the
piezoelectric sonomicrometry crystals (S), creating vibrations and
sending sound pulses toward the receiving crystal (R), which
generates an electric potential induced by the vibrations. The
distance between the crystals (D) is calculated as the time between
the signals sent and received (t.sub.S-t.sub.R) multiplied by the
velocity of the signal (V.sub.s), or
D=(t.sub.S-t.sub.R)V.sub.s.
[0050] One embodiment of the invention incorporates the use of
sensors positioned on endocardial leads for placement in the heart.
This lead-based sonomicrometry (LBS) approach may involve
positioning one transducer in the right ventricular (RV) apex and
the other in the distal coronary sinus (CS), for example, in order
to measure LV Dim, as shown in the system of FIG. 2.
[0051] In FIG. 2, heart 10 includes the upper heart chambers, the
right atrium (RA) and left atrium (LA), and the lower heart
chambers, the right ventricle (RV) and left ventricle (LV), and the
various blood vessels attached thereto. The coronary sinus (CS)
extends from the opening in the RA laterally around the LA and LV
wall to form the great cardiac vein (GV) that extends further
inferiorly into branches of the GV. FIG. 2 also shows a schematic
representation of an implanted, three or four chamber cardiac
pacemaker or monitor or ICD (hereinafter referred to as IPG 14) of
the above-noted types for restoring AV sequential contractions of
the atrial and ventricular chambers and simultaneous or sequential
pacing of the right and left ventricles, and/or for monitoring the
mechanical function of one or more heart chambers and/or delivering
anti-tachyarrhythmia therapies.
[0052] IPG 14 depicted in FIG. 2 is implanted subcutaneously in a
patient's body between the skin and the ribs. Three endocardial
leads 16, 32 and 52 connect the IPG 14 with the RA, the RV and both
the LA and the LV, respectively. Each lead has two electrical
conductors and at least one pace/sense electrode, and a remote
indifferent can electrode 20 may be formed as part of the outer
surface of the housing of the IPG 14. The depicted positions in or
about the right and left heart chambers are merely exemplary.
[0053] In the embodiment of FIG. 2, RA lead 16 is transvenously
passed through the superior vena cava (SVC) and into the RA of the
heart 10, and the distal end of the RA lead 16 is attached to the
RA wall within the RA appendage by an attachment mechanism 24 that
can form one pace/sense electrode. Lead 16 is formed with an
in-line connector 13 fitting into IPG connector block 12. The
in-line connector 13 is coupled to an RA lead conductor pair within
lead body 15 and connected with distal tip RA pace/sense electrode
24 and a proximal ring-shaped RA pace/sense electrode 22. Delivery
of RA pace pulses and sensing of RA sense events may be effected
between the distal tip RA pace/sense electrode 24 and proximal
ring-shaped RA pace/sense electrode 22. Alternatively, a unipolar
endocardial RA lead could be substituted for the depicted bipolar
endocardial RA lead 16. In an embodiment where IPG 14 comprises an
ICD, the RA lead 16 can also include an elongated RA/SVC
cardioversion/defibrillation electrode and associated conductor and
connector element.
[0054] In the embodiment of FIG. 2, RV lead 32 is transvenously
advanced through the SVC and the RA and into the RV where its
distal tip RV pace/sense electrode 40 is fixed in place in the RV
apex by a conventional distal attachment mechanism 41 (which may
also constitute the distal tip pace/sense electrode). The RV lead
32 is formed with an RV lead conductor pair within lead body 36
extending from an in-line connector 34 fitting into IPG connector
block 12. A first conductor of the RV lead conductor pair is
connected with distal tip RV pace/sense electrode 40, and a second
conductor of the RV lead conductor pair is connected with the
ring-shaped RV pace/sense electrode 38. Delivery of RV pace pulses
and sensing of RV sense events may be effected between the distal
tip RV pace/sense electrode 40 and the proximal ring-shaped RV
pace/sense electrode 38. Alternatively, a unipolar endocardial RV
lead could be substituted for the depicted bipolar endocardial RV
lead 32. In the ICD embodiment, the RV lead 32 can also include an
elongated RV cardioversion/defibrillation electrode and associated
conductor and connector element.
[0055] A multi-polar, endocardial CS lead 52 is advanced
transvenously through the SVC, the RA, the ostium of the CS, the CS
itself, and into the GV or a further cardiac vessel branching from
the GV. A pair of distal, ring-shaped, LV/CS pace/sense electrodes
48 and 50 are thus located deep in the GV alongside the LV to allow
delivery of LV pace pulses and sensing of LV sense events. The LV
pacing pulses may be delivered to the LV simultaneously with or in
timed relation with the delivery of pacing pulses to the RV. As
shown in the illustrated embodiment of FIG. 2, LV/CS lead 52 may
also have proximal, ring-shaped, LA/CS pace/sense electrodes 28 and
30 positioned along the CS lead body 56 to lie in the larger
diameter CS adjacent the LA.
[0056] The LV/CS lead 52 is formed with a multiple conductor lead
body 56 coupled at a proximal end connector 54 fitting into IPG
connector block 12. In this case, the CS lead body 56 may encase
electrically insulated LV and LA lead conductor pairs extending
distally from connector elements of a dual bipolar connector 54. A
small diameter lead body 56 may be selected in order to place the
distal LV/CS pace/sense electrode 50 further distal in a vein
branching inferiorly from the GV. In an alternate embodiment, LV/CS
lead 52 could bear a single LA/CS pace/sense electrode 28 and/or a
single LV/CS pace/sense electrode 50 for unipolar operation.
Typically, CS lead 52 does not employ any fixation mechanism and
instead relies on the close confinement within these vessels to
maintain the pace/sense electrode or electrodes or
cardioversion/defibrillation electrode at a desired site. In an
embodiment incorporating an ICD, CS lead 52 can also include an
elongated CS/LV cardioversion/defibrillation electrode and
associated conductor and connector element.
[0057] In accordance with one embodiment of the invention, a sensor
70 may be incorporated within a distal segment of the lead body 56
of LV/CS lead 52 to be located alongside the LV, and a sensor 72
may be incorporated within a distal segment of the lead body 36 of
RV lead 32. An additional sensor 74 may also be located more
proximally on the RA lead body 15 to locate it in the RA or SVC.
Additionally or alternatively, a sensor 74' may be incorporated
within a more proximal segment of the CS lead body 56 of LV/CS lead
52 to be located alongside the LA.
[0058] In one embodiment, sensors 70, 72, and 74 or 74' may
comprise sonomicrometer crystals, as previously noted. The
sonomicrometer crystals can each be formed as a cylindrical
piezoelectric crystal tube sandwiched between an inner tubular
electrode and an outer tubular electrode and fitted around the lead
body 36 of the type described in U.S. Pat. No. 5,795,298. Various
sonomicrometer systems for measuring distance between a
piezoelectric crystal acting as a transmitter of ultrasonic energy,
and a receiving piezoelectric crystal that vibrates and provides an
output signal when exposed to the ultrasonic energy, are disclosed
in U.S. Pat. Nos. 5,779,638, 5,795,298, 5,817,022 and
5,830,144.
[0059] In the embodiment shown in FIG. 2, the LA lead conductors of
LV/CS lead 52 that are connected to the more proximal LA CS
pace/sense electrodes 28 and 30 may also be connected to the
electrodes of the sonomicrometer crystal 74'. Similarly, the LV
lead conductors of LV/CS lead 52 that are connected to the more
distal LV CS pace/sense electrodes 50 and 48 may also be connected
to the electrodes of the sonomicrometer crystal 70. The RV lead
conductors of RV lead 32 that are connected to the RV pace/sense
electrodes 40 and 38 may also be connected to the electrodes of the
sonomicrometer crystal 72. The RA lead conductors of RA lead 16
that are connected to the RA pace/sense electrodes 24 and 22 may
also be connected to the electrodes of the sonomicrometer crystal
74.
[0060] An electrode of the piezoelectric crystals 70, 72, 74, and
74' may also be employed as an indifferent pace/sense electrode to
provide bipolar pacing and sensing, replacing the indifferent
ring-shaped pace/sense electrodes on the same lead body. The
piezoelectric crystals 70, 72, 74, and 74' can be located distal to
or between pace/sense electrodes or proximal to the pace/sense
electrode or electrodes as shown. The particular depicted locations
and relative sizes and spacings between pace/sense electrodes and
sonomicrometer crystals are not necessarily to scale and are
exaggerated for convenience of illustration.
[0061] In certain embodiments of the invention, IPG 14 may comprise
an ICD and one or more of the leads 16, 32 and 52 may also
incorporate cardioversion/defibrillation electrodes and lead
conductors extending thereto through the lead bodies for delivering
atrial and/or ventricular cardioversion/defibrillation shocks in
any of the configurations and operating modes known in the art.
[0062] The sonomicrometer crystals 70, 72, 74 and 74' are thereby
disposed apart by the RV-LV distance (denoted as D1 in FIG. 2), the
LV-RA distance (denoted as D2 in FIG. 2), the RV-RA distance
(denoted as D3 in FIG. 2), and the RV-LA distance (denoted as D4 in
FIG. 2). The RV-LV distance (D1) between the RV and LV crystals
provides a measure of LV dimension (LV Dim), and changes in the LV
Dim signal over a cardiac cycle are strongly correlated with
changes in LV volume as the LV fills during diastole and empties
during systole. Alternately, the RV-LA distance (D2) between the RV
and LA crystals may also provide a measure of LV Dim in certain
embodiments of the invention, possibly as a back-up to D1, or
possibly to augment the information from D1.
[0063] FIG. 3 shows the relationship between the LV Dim signal
(labeled "LV-RV" in FIG. 3) and an electrocardiogram signal (ECG)
for a heart in normal sinus rhythm. The peak of the LV Dim signal
occurs at the point labeled "max LV-RV" and identifies the
beginning of the systolic function (ejection) of the heart. The
point labeled "min LV-RV" identifies the end of the systolic
function and the beginning of the diastolic function (filling) of
the heart.
[0064] FIG. 4 shows an example of the LV Dim signal as a function
of time over a cardiac cycle, as well as the first derivative of LV
Dim with respect to time. The LV Dim signal shown in FIG. 4 spans a
single cardiac cycle, comprising a ventricular filling phase and a
ventricular ejection phase. The transition from the filling phase
to the ejection phase is also indicated in FIG. 4. In addition to
information about systolic function (ejection), diastolic function
(filling), and extent of filling (preload), this signal may also
contain information about the synchrony or effectiveness of LV
contraction during the isovolumic contraction phase. The isovolumic
contraction phase is identified in FIG. 4 as the time period
between the two vertical dashed lines. This phase begins with
closure of the mitral valve (first dashed line) and ends with
opening of the aortic valve (second dashed line), and is
characterized by a sudden increase in left ventricular pressure
(not shown in FIG. 4).
[0065] The shape of the LV Dim signal is correlated with changes in
LV volume over a cardiac cycle, while the shape of the first
derivative of the LV Dim signal (labeled "dLVD/dt") is analogous to
mitral valve flow during ventricular filling and inverse aortic
flow during ejection. Thus, the LV Dim signal and its derivative
contain important information about cardiac performance, including
diastolic function, systolic function and synchrony of ventricular
contractions.
[0066] As noted above, "isovolumic contraction" occurs during the
transition between ventricular filling and ejection, and is
characterized by a sharp increase in pressure within the ventricle
due to the contraction of the ventricle following closure of the
mitral valve and prior to opening of the aortic valve. The
isovolumic contraction phase of a normal cardiac cycle may be
illustrated on a pressure vs. volume plot and is shown as the solid
vertical line in FIG. 5, which displays LV pressure versus LV
volume over a cardiac cycle. A cardiac cycle follows the somewhat
rectangular path shown in FIG. 5. The point labeled 101 corresponds
to the opening of the mitral valve, which allows blood to begin
flowing into the LV. As blood continues to flow into the LV, the LV
expands in volume, corresponding to line segment 111, which
represents ventricular filling. At 102, the mitral valve closes,
ending the filling phase and beginning the isovolumic contraction
phase. Between mitral valve closure 102 and aortic valve opening
103, the LV begins to contract, but due to the near
incompressibility of liquids (i.e., blood), LV pressure rises
sharply during isovolumic contraction, as indicated by segment 112.
From aortic valve opening 103 to aortic valve closure 104, blood is
rapidly ejected at high pressure from the LV to the aorta (line
segment 113). The end of the ventricular contraction and the
closure of the aortic valve causes LV pressure to rapidly decrease
until the mitral valve again opens at 101 to begin another cardiac
cycle.
[0067] FIG. 6 shows examples of cardiac cycles for a number of
different pacing lead locations. The isovolumic contraction phase
of several of these plots reveal shape changes that are indicative
of a reduction in ventricular performance. For example, 120 shows a
decrease in the LV volume at the beginning of isovolumic
contraction, indicating possible LV asynchrony for this lead
configuration. 124 indicates that for this particular lead
configuration (bi-ventricular pacing at the RV septal wall and in
the LV), a relatively straight/vertical isovolumic contraction has
occurred, possibly showing that ventricular synchrony has been
improved or restored, which should result in improved hemodynamics
for the patient.
[0068] Asynchronous contraction of the left ventricle may lead to
mitral valve regurgitation and/or isovolumic shape changes of the
LV. Either of these effects may be detected upon observation of
changes in LV volume, either real or apparent. For example, mitral
valve regurgitation may result in an actual decrease in LV Volume,
whereas a shape change of the LV may cause measured LV Volume to
change without an actual decrease in LV Volume. Since the LV Dim
signal is highly correlated to LV volume, ventricular performance
may be evaluated by analysis of certain features of the LV Dim
signal that may be manifestations of either mitral valve
regurgitation or isovolumic shape changes of the LV.
[0069] Measurement of the LV Dim signal as a function of time,
using means such as lead-based sonomicrometry (LBS), permits
calculation of two novel indices of ventricular performance. FIG. 7
is an enlarged drawing of a portion of the signals shown in FIG. 4.
The LV Dim signal in FIG. 7 illustrates the measurement of two
indices of ventricular performance, "premature shortening" (PS) and
"isovolumic lengthening" (IL). PS and IL are quantitative indices
of ventricular performance that can be derived and measured from
the LV Dim signal as described below.
[0070] Premature shortening (PS) is defined as the decrease in LV
Dim from a first local maximum 130 near end-diastole associated
with mitral valve closure to a local (relative) minimum or
inflection point 132. PS is shown in FIG. 7 as the decrease in LV
Dim from the first peak 130 to the "dip" 132 in the LV Dim signal.
Isovolumic lengthening (IL) is defined as the increase in left
ventricular dimension from the local (relative) minimum 132 to a
second local maximum 134 at or near the time of aortic valve
opening. IL is shown in FIG. 7 as the increase in LV Dim from the
"dip" 132 to the second peak 134 in the LV Dim signal. In a normal,
synchronous LV contraction, both PS and IL would have values at or
near zero.
[0071] One of ordinary skill in the art will appreciate that
measurement of PS and IL may be accomplished by equivalent
mathematical means. For example, the derivative of the LV Dim
signal may be mathematically integrated over the period of time
corresponding to PS or IL to determine the same numerical values. A
mathematical integration may, for example, calculate the area of
the shaded regions 135, 136, yielding values that correspond to or
are equivalent to the measured values of PS and IL, respectively,
determined directly from the LV Dim signal. Such equivalent
mathematical techniques of measuring the values of PS and IL are
contemplated and are understood to fall within the scope of the
invention.
[0072] Referring again to FIG. 6, it was noted that the isovolumic
contraction portion of the curve may provide information regarding
ventricular performance, including the presence of LV asynchrony.
The relationship between the pressure-volume curves of FIG. 6 and
the PS and IL values determined from a corresponding LV Dim
measurement discussed above is described in FIGS. 8 and 8(a), where
portions of the isovolumic contraction segment of representative LV
pressure-dimension curves have been enlarged. In the example of
FIG. 8, a decrease in LV dimension occurs during isovolumic
contraction, corresponding to the premature shortening (PS) of the
LV. In the example of FIG. 8(a), a decrease followed by an increase
in the LV dimension during isovolumic contraction is shown,
corresponding to both the PS and IL of the LV Dim signal,
respectively. Thus, the LV Dim signal contains some of the same
information about ventricular performance that can be obtained by
measuring LV pressure and LV volume over a cardiac cycle, but is
amenable to a simpler lead-based measurement, such as by lead-based
sonomicrometry (LBS). Further, the measurement of LV Dim may be
accomplished by a chronically implanted lead-based system, with PS
and IL measurements calculated and stored by an IMD, or used in an
algorithm by an IMD to attempt to optimize ventricular performance,
either automatically (on a periodic, on-going basis, for example),
or by an operator using external equipment to communicate with an
IMD, for example to re-program pacing parameters based on stored
values of PS and IL retrieved from the IMD.
[0073] Changes in the values of PS and IL (and hence in ventricular
performance) may be associated with variations in the programmed
atrio-ventricular (AV) delay in a paced heart, as well as with
variations in the location of ventricular pacing leads, as shown in
FIGS. 9 and 10, respectively. Variations in inter-ventricular
pacing delay (V-V) between the left and right ventricles may also
affect synchrony in bi-ventricularly paced hearts. By using PS and
IL to optimize the location of pacing sites and to adjust the AV
and V-V delays, ventricular performance may be optimized and the
heart may provide improved cardiac output. Hence, measuring PS and
IL may provide the ability to optimize ventricular performance both
at the time of implantation of a pacing system, as well as
post-implant, either automatically or manually using PS and IL
data.
[0074] In one possible embodiment of the invention, multi-site
pacing leads may be employed in conjunction with an IMD pacing
system. Multi-site pacing leads, as are known in the art, provide
the ability to vary the pacing site in a chronically implanted
lead. FIG. 11 shows an embodiment of the invention that
incorporates multi-site pacing leads for RV lead 232 and the LV/CS
lead 252. For example, RV lead 232 has the ability to pace and/or
sense from any pair of electrodes 141, 140, 138, 142, 143, 144, and
145. To change the pacing site location, for example, an operator
may be able to select the pacing site between the fixation tip
electrode 141 and ring electrode 140 in order to select the RV
septal wall as one of the pacing site locations. An operator may
make measurements of PS and IL with the RV septal wall as the
pacing site location, for example, then select a new pacing site
location, such as between ring electrodes 142 and 143, to evaluate
the impact or change on measured values of PS and IL. Similarly,
the LV/CS lead 252 may have the ability to pace from multiple
sites. For example, pacing and sensing may be selected to occur
between ring electrodes 148 and 150 for an initial measurement of
PS and IL, for comparison with PS and IL measurements made using an
alternate pacing site location, such as between ring electrodes 153
and 154.
[0075] Another embodiment of the invention comprises an IMD with
the ability to automatically vary the pacing site locations in
either or both the RV lead 232 and the LV/CS lead 252 in order to
attempt to minimize the measured values of PS and/or IL, and to
thereby improve ventricular performance. Thus, an embodiment of the
invention includes the ability to vary the pacing site location(s)
in response to measured values of PS and IL to attempt to improve
ventricular performance.
[0076] In an alternate embodiment of the invention, sensors 70, 72,
74, and 74' may be placed on temporary catheters or guide wires,
for example, to evaluate ventricular performance during lead
placement and to determine optimum lead locations to maximize
ventricular performance by attempting to minimize the measured
values of PS and IL. FIGS. 12 and 13 show this technique being
employed for an RV lead and an LV lead, respectively. FIG. 12 shows
the use of temporary transducer catheters for measuring values of
PS and IL at the time of implantation of an RV lead. As shown in
FIG. 12, the temporary transducer catheters may be used to position
sensors at the points labeled T1 and T2. The RV lead may then be
repeatedly repositioned, measuring PS and IL values at each pacing
site location. In this manner, a pacing site location for the RV
lead may be chosen that achieves values of PS and/or IL that
optimize ventricular performance. Upon finding an optimal pacing
site location and affixing the RV lead, the temporary transducer
catheters may be removed from the patient's heart.
[0077] FIG. 13 shows a similar arrangement for placing a LV lead.
Temporary transducer catheters may be employed as described above
to position sensors at locations T1 and T2. Alternately, a guide
sheath may be used as shown in FIG. 13 to both position a sensor in
the coronary sinus, and allow movement of the LV/CS pacing lead
longitudinally relative to the guide sheath, for example. Upon
determination of a suitable pacing site location for the LV/CS
lead, the guide sheath of this embodiment may be removed from the
patient's heart. The LV lead, for example, may be slidably guided
within a lumen in the guide sheath, as shown in FIG. 13. The guide
sheath may include a sensor, such as a piezoelectric sonomicrometry
crystal, attached to the guide sheath and held in a relatively
stable position within the CS to allow measurements of LV Dim, PS,
and IL for different locations of the pace/sense electrode(s) of
the LV lead.
[0078] Acute measurements of PS and IL, such as provided by
temporary transducer catheters with sensors affixed thereto, have
the potential benefit of resulting in a system with fewer
chronically implanted components. The acute measurements of PS and
IL, and the related measurements made at time of implant regarding
changes in PS and IL as a function of varying pacing parameters,
may comprise sufficient information for the long-term management of
an IMD without the need for further measurements of PS and IL. This
may result in an IMD system that is easier to monitor and
follow-up. Alternately, sensors implanted chronically for
continuing measurements of PS and IL during the chronic operation
of an IMD may prove to be beneficial in monitoring and evaluating
the long-term progress of the patient's heart condition. For
example, anecdotal evidence may suggest that "remodeling" of the
heart may occur over time due to the improved hemodynamics provided
by optimizing ventricular performance. Such remodeling may allow
for a series of on-going, future adjustments to further improve
ventricular performance, for example. Thus, a clinician/physician
may decide that the benefit of having the ability to monitor and
evaluate ventricular performance chronically using an IMD may
outweigh any added complexity associated with the sensors and lead
system necessary to provide this information.
[0079] FIG. 14 shows a block diagram of a method for operating an
IMD to optimize ventricular performance. The first step in the
method is to measure PS and/or IL based on measuring LV Dim over
one or more cardiac cycles. An optional step (not shown) may be to
derive a criterion from the measured values of PS and/or IL. Such a
criterion may be selected by an operator, and may consist of the
value of PS by itself, IL by itself, or some weighted function of
both PS and IL, for example a weighted average of the two indices.
The next step is to adjust a pacing parameter, such as the AV
delay, VV delay, pacing mode, pacing rate, pacing site location,
etc., possibly based on the measured values of PS and/or IL, or on
the criterion derived therefrom. The next step in the method is to
measure PS and/or IL after the adjustment in pacing parameter, to
(optionally) derive a new criterion from the measured values of PS
and/or IL, and determine if there has been an improvement or a
worsening in the PS, IL, or criterion values. The last step in the
method is to continue adjusting one or more of the pacing
parameters until the criterion has been improved to an optimal
level, or until no further improvement is possible, then ending the
adjustment.
[0080] FIG. 15 illustrates an example of a screen shot from a
programming device designed to communicate with the IMD via RF
telemetry, for example, according to a possible embodiment of the
invention. The screen shot in FIG. 15 provides an operator with a
real time display of the ECG, LV Dim, and d(LVD)/dt signals, with
constantly updating measured values for PS, IL and any criterion of
ventricular performance or synchrony determined from the measured
values of PS and IL. Furthermore, the programmer's screen may have
user-operated buttons, such as touch screen controls, that allow
for changes to paced programming parameters (such as AV Delay, V-V
Delay, etc.), while watching a real time update in the values of
PS, IL, and any ventricular performance criterion. The programmer
interface of FIG. 15 would allow an operator to attempt to optimize
ventricular performance, both at the time of implant and
post-implant, such as at a patient follow-up visit. At the time of
implant, for example, the LV Dim signal and its first derivative
may be provided by either an acute/temporary sensor system, or by a
sensor configuration that is incorporated into the pacing leads.
For post-implant use, the IMD could rely on sensor signals from a
chronically implanted sensor system, such as those illustrated in
FIG. 1, obviating the need for an invasive procedure to place
sensors.
[0081] The screen shot of FIG. 15 provides a programmer interface
that allows an operator (physician, etc.) to interact with an
appropriately equipped IMD (i.e., via RF telemetry, for example)
and lead system to measure PS and IL, determine a criterion of
ventricular performance therefrom, and make adjustments to pacing
parameters and/or pacing site locations in order to achieve a
"best" criterion value for the particular heart/patient and thereby
maximize ventricular performance for the patient.
[0082] Thus, embodiments of a METHOD AND APPARATUS FOR EVALUATING
VENTRICULAR PERFORMANCE DURING ISOVOLUMIC CONTRACTION are
disclosed. One skilled in the art will appreciate that the present
invention can be practiced with embodiments other than those
disclosed. The disclosed embodiments are presented for purposes of
illustration and not limitation, and the present invention is
limited only by the claims that follow.
* * * * *